All eucaryotic cells can experience breaks within their chromosomes which must be repaired efficiently to retain viability. Such broken chromosomes arise both spontaneously and after exposure to endogenous and exogenous agents. Treatments which have been shown to cause DNA strand breaks include physical agents (e.g. X-rays) and chemical agents (e.g. methylmethane sulfonate, anti-tumor drugs such as phleomycin or bleomycin, etc.). Double-strand breaks within DNA stimulate mutagenesis, recombination, and aneuploidy and are, therefore, implicated in the etiology of both carcinogenesis and aging. The model eucaryote Saccharomyces cerevisiae has been used to study genes involved in the repair of broken chromosomes and which mediate recombination events that occur during normal mitotic growth. Several genes known to be involved in these processes (including rad50, rad51, rad52, and others) have been characterized in great detail. In addition, several newly identified mutants have been shown to affect the same pathways of DNA repair and recombination. These mutants have been analyzed for their sensitivity to specific mutagens, spontaneous and induced recombination proficiency, and their ability to repair DNA strand breaks induced by in vivo expression of the HO, EcoRI, and PvuII endonucleases.